Plasma Catechol Amine Concentrations in Myocardial Infarction and Angina Pectoris

Gazes, Peter C.; Richardson, James A.; Woods, E. F.

doi:10.1161/01.cir.19.5.657

Cited by 200 publications

(27 citation statements)

References 19 publications

(1 reference statement)

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“…In man during insulin hypoglycaemia (Holzbauer & Vogt, 1954), the concentration of catecholamines in plasma reaches levels not far below those at which potentiation is observed in vitro. The concentration is also increased shortly after myocardial infarction (Gazes, Richardson & Woods, 1959) at a time when platelet adhesiveness is increased (McDonald & Edgill, 1959). Thus the levels of catecholamines in the plasma may be one of the factors controlling platelet aggregation, at least under pathological conditions.…”

Section: Discussionmentioning

confidence: 99%

Effects of adrenaline on human blood platelets

Mills¹,

Roberts²

1967

The Journal of Physiology

286

107

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SUMMARY1. Adrenaline at concentrations too low to cause aggregation of human platelets potentiates the aggregation by adenosine diphosphate. Noradrenaline has the same effect but is less active than adrenaline; isopropylnoradrenaline is inactive or inhibitory.2. The potentiation of adenosine diphosphate by catecholamines is blocked by the adrenergic ac-receptor antagonists phentolamine and dihydroergotamine but not by 2-halogenoethylamines or by adrenergic fl-receptor antagonists.3. Both the first and second phases of adenosine diphosphate aggregation are potentiated by catecholamines but the second phase more than the first.4. The release from the platelets of adenine nucleotides which is associated with the second phase of aggregation is also increased by adrenaline.

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Section: Discussionmentioning

confidence: 99%

Effects of adrenaline on human blood platelets

Mills¹,

Roberts²

1967

The Journal of Physiology

286

107

View full text Add to dashboard Cite

show abstract

“…[9][10][11][12][13][14] Patients with acute myocardial infarction frequently exhibit excessive adrenergic activity as evidenced by an elevation of plasma and 24-hour urinary catecholamines. [15][16][17][18][19][20][21][22][23] It was therefore hypothesized that the abbreviated electromechanical systole characteristic of patients with myocardial infarction is a direct reflection of increased sympathetic nervous system activity. The.present investigation was designed to test this hypothesis.…”

Section: Ine Excretionmentioning

confidence: 99%

Shortening of Electromechanical Systole as a Manifestation of Excessive Adrenergic Stimulation in Acute Myocardial Infarction

et al. 1972

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“…Therefore, an increase in LVEDP and tachycardia apparently represent compensatory mechanisms by which cardiac output is maintained after severe myocardial infarction. A positive inotropic effect of reflex sympathoadrenal activation may also play a role in supporting cardiac performance (29). These observations suggest that the patients with clinical signs of heart failure had more severe impairment of left ventricular performance, but the data do not permit conclusions as to whether the cardiac dysfunction is due to: (a) a larger noncontracting area of myocardium; (b) paradoxical pulsations (dyskenesia) of the infarcted area; or (c) failure of the uninvolved myocardium to adequately compensate by increased fiber shortening (30).…”

Section: Left Ventricular Function In Acute Myocardial Infarctionmentioning

confidence: 99%

Left ventricular function in acute myocardial infarction

Hamosh¹,

Cohn

1971

J. Clin. Invest.

125

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A B S T R A C T Left ventricular catheterization was carried out in 40 patients with acute myocardial infarction. Left ventricular end-diastolic pressure (LVEDP) was elevated in 85% of the patients studied. In 14 patients with apparently uncomplicated infarcts, LVEDP averaged 15 mm Hg, and cardiac index (2.98 liter/min/m'), stroke volume (38.3 ml/m'), and stroke work (49.2 g-m/m') were within normal limits. In 12 patients with clinical signs of left ventricular failure, LVEDP averaged 29.9 mm Hg, cardiac index was at the lower limit of normal (2.79 liter/min/m'), but stroke volume (31.6 ml/m') and stroke work (37.3 g-m/m') were reduced.In 14 patients with clinical signs of shock, LVEDP averaged significantly lower than in the heart failure group (21.1 mm Hg), but cardiac index (1.59 liter/min/ m'), stroke volume (16.5 ml/m'), and stroke work (11.1 g-m/m') were markedly reduced. A large presystolic atrial "kick" (average amplitude 9.5 mm Hg) was an important factor in the high LVEDP in the patients with heart failure but not in those with shock. The first derivative of left ventricular pressure was significantly lower in shock than in the nonshock group. Although right atrial pressure (RAP) and LVEDP were significantly correlated (r = 0.49), wide discrepancies in individual patients rendered the RAP an unreliable indicator of the magnitude of left ventricular filling pressure.These data show the following: (a) LVEDP is usually elevated in acute myocardial infarction, even in absence of clinical heart failure; (b) cardiac output apparently is supported by increased LVEDP and compensatory tachycardia; (c) in patients with shock, left ventricular function usually is markedly impaired, but inadequate compensatory cardiac dilatation or tachycardia could contribute to the reduced cardiac output in some indiThis work was presented in part at the meeting of The

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Plasma Catechol Amine Concentrations in Myocardial Infarction and Angina Pectoris

Cited by 200 publications

References 19 publications

Effects of adrenaline on human blood platelets

Effects of adrenaline on human blood platelets

Shortening of Electromechanical Systole as a Manifestation of Excessive Adrenergic Stimulation in Acute Myocardial Infarction

Left ventricular function in acute myocardial infarction

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